Renal Oxygen Delivery and Consumption during Progressive Hypoxemia in the Anesthetized Dog

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Abstract
The relationship between renal O2 delivery (RDO2) and function was evaluated during progressive hypoxemia. Seven anesthetized, spontaneously breathing dogs were given progressively lower oxygen concentrations to breathe while monitoring renal O2 consumption (R.ovrhdot.VO2), renal hemodynamic and excretory function. Basal R.ovrhdot.VO2 was determined in three models of kidneys without filtration. RDO2 averaged 3648 .mu.mole O2/min/100 g during normoxia. Basal R.ovrhdot.VO2 averaged 100 .mu.mol O2/min/100 g kidney while total R.ovrhdot.VO2 was 466 .mu.mole O2/min/100 g kidney during normoxia, leaving 366 .mu.mol O2/min/100 g consumed by those processes involved in tubular transport. During hypoxemia, all renal parameters were well maintained until the lowest PaO2 [partial pressure of arterial O2] (24.2 Torr). At this level, total R.ovrhdot.VO2 and RDO2 were significantly reduced. RDO2 remained well above R.ovrhdot.VO2 throughout hypoxemia. The reduction in R.ovrhdot.VO2 was a direct result of decreased O2 demand, as glomerular filtration and tubular load were also reduced. This associated decrease in O2 demand and R.ovrhdot.VO2 was indicated by the fact that the renal (a-v)O2 difference remained low and unchanged (1.9 vol%), fractional Na excretion was unchanged, and the ratio of tubular Na reabsorption to R.ovrhdot.VO2 also remained unchanged (30.8 meq Na/mmole O2). Hypoxemia, while reducing both RDO2 and R.ovrhdot.VO2 at the lowest PaO2 (24.2 Torr), did not functionally impair renal excretory function by limiting RDO2 to the tubular transport processes. A reduction in RBF is far more likely to compromise the RDO2 needed to sustain basal and active transport processes than hypoxemia itself.

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